IBIOBA - MPSP   22718
INSTITUTO DE INVESTIGACION EN BIOMEDICINA DE BUENOS AIRES - INSTITUTO PARTNER DE LA SOCIEDAD MAX PLANCK
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
PIAS4 IMPAIRS TAU HOMEOSTASIS
Autor/es:
SOKN CLARA; BUDZIÑSKI MAIA LUDMILA; ERDOCIA MARIANA; SOKN CLARA; BUDZIÑSKI MAIA LUDMILA; ERDOCIA MARIANA; UGO BELEN; ATTORRESI ALEJANDRA; ARZT EDUARDO; UGO BELEN; ATTORRESI ALEJANDRA; ARZT EDUARDO; GOBBINI ROMINA; SENIN SERGIO; LIBERMAN ANA CLARA; GOBBINI ROMINA; SENIN SERGIO; LIBERMAN ANA CLARA
Reunión:
Congreso; LXV Reunión Anual de la Sociedad Argentina de Investigación Clínica; 2020
Institución organizadora:
Sociedad Argentina de Investigación Clínica
Resumen:
Tauopathies are neurodegenerative diseases characterized by the formation of intracellular hyperphosphorylated tau deposits. Notably, aberrant tau accumulation in brain often co-occurs with other protein aggregates, suggesting that there might be common factors supporting their deregulation. Accumulating evidence points to the PIAS SUMO E3-ligases as SUMOylation inductors of several key proteins involved in neurodegeneration, modifying their solubility, activity, or stability. Taking this into account, we hypothesize that these enzymes could be common regulatory factors implicated in neurodegenerative processes. The aim of this work is to determine the role of PIAS family in the regulation of tau protein homeostasis. By means of a western blot (WB)-based screening in HT22 cells overexpressing human 2N4R WT tau (hTau) together with PIAS family members, we observed that only PIAS4 increased total tau levels (+1.75, p